Avascular necrosis

In many cases, there is pain and discomfort in a joint which increases over time. It can affect any bone, and in about half of affected people, multiple sites are damaged. Avascular necrosis most commonly affects the ends of long bones, such as the femur. Other common sites include the humerus (upper arm), knees, shoulders, ==Causes==

The main risk factors are bone fractures, joint dislocations, alcoholism, and the use of high-dose steroids. HIV infection, Gaucher's disease, and Caisson disease (dysbaric osteonecrosis). Bisphosphonates are associated with osteonecrosis of the mandible (jawbone). The condition may also occur without any clear reason. In children, avascular osteonecrosis can have several causes. It can occur in the hip as part of Legg–Calvé–Perthes syndrome, and it can also occur as a result after malignancy treatment such as acute lymphoblastic leukemia and allotransplantation. ==Pathophysiology==

The hematopoietic cells are most sensitive to low oxygen and are the first to die after reduction or removal of the blood supply, usually within 12 hours. Experimental evidence suggests that bone cells (osteocytes, osteoclasts, osteoblasts etc.) die within 12–48 hours, and that bone marrow fat cells die within 5 days. Upon reperfusion, repair of bone occurs in two phases. First, there is angiogenesis and movement of undifferentiated mesenchymal cells from adjacent living bone tissue grow into the dead marrow spaces, as well as entry of macrophages that degrade dead cellular and fat debris. Second, there is cellular differentiation of mesenchymal cells into osteoblasts or fibroblasts. Under favorable conditions, the remaining inorganic mineral volume forms a framework for establishment of new, fully functional bone tissue. ==Diagnosis==

(epiphyseal plates are open): arrows point to avascular necrosis and developing osteochondritis dissecans in the outer medial condyle of femur In the early stages, bone scintigraphy and MRI are the preferred diagnostic tools. X-ray images of avascular necrosis in the early stages usually appear normal. In later stages it appears relatively more radio-opaque due to the nearby living bone becoming resorbed secondary to reactive hyperemia. File:Pathology of avascular necrosis.jpg|Pathology of avascular necrosis, with a photograph of a cross-section of the involved bone at top left. The reactive zone shows irregular trebaculae with empty lacunae, and fibrosis of the marrow space. Types When AVN affects the scaphoid bone, it is known as Preiser disease. Another named form of AVN is Köhler disease, which affects the navicular bone of the foot, primarily in children. Yet another form of AVN is Kienböck's disease, which affects the lunate bone in the wrist. ==Treatment==

A variety of methods may be used to treat the disease, Other techniques, such as metal-on-metal resurfacing, may not be suitable in all cases of avascular necrosis; its suitability depends on how much damage has occurred to the femoral head. Bisphosphonates, which reduce the rate of bone breakdown, may prevent collapse (specifically of the hip) due to AVN. Core decompression Other treatments include core decompression, whereby internal bone pressure is relieved by drilling a hole into the bone, and a living bone chip and an electrical device to stimulate new vascular growth are implanted; and the free vascular fibular graft (FVFG), in which a portion of the fibula, along with its blood supply, is removed and transplanted into the femoral head. A 2016 Cochrane review found no clear improvement between people who have had hip core decompression and participate in physical therapy, versus physical therapy alone. There is additionally no strong research on the effectiveness of hip core decompression for people with sickle cell disease. ==Prognosis==

The amount of disability that results from avascular necrosis depends on what part of the bone is affected, how large an area is involved, and how effectively the bone rebuilds itself. The process of bone rebuilding takes place after an injury as well as during normal growth. and the joint surface breaks down, leading to pain and arthritis. ==Epidemiology==

Avascular necrosis usually affects people between 30 and 50 years of age; about 10,000 to 20,000 people develop avascular necrosis of the head of the femur in the US each year. ==Society and culture==

Cases of avascular necrosis have been identified in a few high-profile athletes. It abruptly ended the career of American football running-back Bo Jackson in 1991. Doctors discovered Jackson to have lost all of the cartilage supporting his hip while he was undergoing tests following a hip injury he had on the field during a 1991 NFL Playoff game. Avascular necrosis of the hip was also identified in a routine medical check-up on quarterback Brett Favre following his trade to the Green Bay Packers in 1992. However, Favre would go on to have a long career at the Packers. Another high-profile athlete was American road racing cyclist Floyd Landis, winner of the 2006 Tour de France, the title being subsequently stripped from his record by cycling's governing bodies after his blood samples tested positive for banned substances. During that tour, Landis was allowed cortisone shots to help manage his ailment despite cortisone also being a banned substance in professional cycling at the time. Rafael Nadal successfully continued his tennis career after having surgery for Mueller–Weiss syndrome (osteonecrosis of the navicular bone in the foot). YouTuber Steve Wallis has revealed that he has the condition in his hip. == See also ==